Chapter 3- Pathology Flashcards
(161 cards)
1
Q
What are the 3 diff types of angina?
A
- Stable angina
- Unstable angina
- Prinzmetal (or variant) angina
2
Q
In what situations do stable angina arise?
A
Exertion
Emotional stress
3
Q
What is the main etiology of stable angina
A
Stable atherosclerotic plaque within the coronary arteries with > 70% stenosis
4
Q
Does stable angina represent reversible or irreversible myocardial injury?
A
Reversible injury
No necrosis
5
Q
What is the classic presentation of stable angina?
A
- Chest pain <20 minutes that radiates to the left arm or jaw (typically 5-10mins)
- Diaphoresis
- Shortness of breath
6
Q
What is the classic ECG finding in stable angina?
A
ST segment depression due to subendocardial ischemia
7
Q
What relieves stable angina?
A
Rest
Nitroglycerin
8
Q
Under what circumstances does unstable angina arise?
A
At rest
9
Q
What is the etiology of unstable angina?
A
Rupture of an atherosclerotic plaque—thrombosis—INCOMPLETE OCCLUSION of coronary artery. (Typically >90% occlusion of coronary artery)
10
Q
Is the injury of unstable angina reversible or irreversible?
A
Reversible injury to myocytes No necrosis (Troponin levels are not elevated)
11
Q
What is the classic ECG finding in unstable angina?
A
ST segment depression due to subendocardial ischemia and/ or T wave inversion
12
Q
What relieves unstable angina?
A
Nitroglycerin
13
Q
What is a possible complication/sequelae of unstable angina?
A
MI
14
Q
Under what circumstances does prinzmetal angina arise?
A
No predisposing circumstance
Episodic chest pain unrelated to exertion (occurs especially at night or early in the morning)
15
Q
What causes prinzmetal angina?
Give 4 exogenous drugs/ substances that can trigger vasospasm
Why do women who have had of variant angina often have a history of migraine headache?
What drug is useful in confirming the diagnosis of prinzmetal angina?
A
- Coronary artery vasospasm
- Cocaine, Triptan, tobacco, ergonovine (these agents induce vasoconstriction)
- Both migraine headache and prinzmetal angina are both associated with arterial vasospasms.
- Ergonovine triggers vasospasm in susceptible patient (used to induce uterine contraction and cessation of bleeding post partum)
16
Q
Is the injury sustained by prinzmetal angina reversible/irreversible?
A
If episode occurs for <20m= reversible injury w/ no necrosis
If episode >20 mins= reversible w/ necrosis
17
Q
What is the ECG finding in prinzmetal angina?
A
ST segment elevation due to transmural ischemia
18
Q
What relieves attack of prinzmetal angina?
A
Nitroglycerin
Ca channel blockers i.e diltiazem (to relieve vasospasm)
19
Q
What is the single most common risk factor for developing Ischemic heart disease?
What causes ischemic heart disease?
A
Atherosclerosis
Compromised blood flow in the coronary vessels
- decreased arterial perfusion
- decreased venous drainage and build up of toxic metabolites
20
Q
What are the 4 types of Ischemic Heart Disease (ICH)
A
- Angina
- MI
- Sudden Cardiac Death
- Chronic Ischemic Heart Disease
21
Q
What is myocardial infarction
A
Necrosis of cardiac myocytes
22
Q
What are the etiologic processes involved in MI?
A
Rupture of atherosclerotic plaque
Subsequent thrombosis
COMPLETE OCCLUSION of coronary artery
Other causes include:
Coronary artery vasospasm (due to prinzmetal angina or cocaine)
Emboli
Vasculitis (of coronary arteries i.e Kawasaki disease)
23
Q
What is the clinical presentation of MI?
A
Severe crushing chest pain >20mins
Radiates to the L. arm and jaw
Diaphoresis
Dyspnea
24
Q
Does nitroglycerin relieve MI?
What is the most common cause of death in MI in the pre-hospital phase?
What is the most common cause of death from MI in the in-hospital phase?
A
NO
Ventricular fibrillation
Ventricular failure and subsequent cardiogenic shock
25
Which areas of the heart are most commonly affected my MI?
Which areas of the heart are generally spared?
1. Left ventricle
2. Right ventricle
Both atria
26
What are the 3 most commonly affected coronary arteries in MI in order of hierarchy
1. Left Anterior Descending Artery (LAD) 45%
- Infarction of anterior wall of the LV
- Infarction of anterior septum of the LV
2. Right Coronary Artery (RCA)
- Infarction of Posterior wall of LV
- Infarction of posterior septum
- Infarction of papillary muscles of LV
3. Left Circumflex Artery (LCX)
- Infarction of lateral wall of LV
27
What form of cardiac mm necrosis is found at the initial stage of MI?
Subendocardial necrosis involving <50% of the wall thickness (Submyocardial infarction)
ST depression on ECG
28
What form of cardiac mm necrosis is found in continued or severe MI?
Transmural necrosis (Transmural infarction)
ST segment elevation
29
What is the most sensitive and specific marker (gold standard) for MI.
What does its levels RISE, PEAK, and NORMALIZE
Troponin I
Rise 2-4hrs after MI
Peak 24 hrs after MI
Return to normal: 7-10 days after MI
30
Which lab test is useful for detecting re-infarction that occurs days after MI? (3-10days)
1. When does it RISE, PEANK and NORMALIZE?
2. Why is CK-MB not as specific as Troponin?
3. What is the function of CK-MB?
CK-MB (Creatine Kinase MB
Rise 4-6 hrs
Peak 24 hrs
Normalize- 72 hrs (3days)
Because it is produced by both cardiac and skeletal muscle
Transfers phosphate group from Creatine Kinase to ADP
31
What are the treatment for (Non-ST elevation MI)& Unstable angina?
What are the treatment for STEMI?
How is pain control achieved in unstable angina, STEMI & NSTEMI?
1. Aspirin/(LMW)heparin, Clopidogrel- Limits thrombosis
2. Supplemental 02- Minimizes ischemia
3. Nitrates- Vasodilate coronary arteries
- Decrease systemic venous resistance by venodilation---Reducing pre-load---Reducing cardiac work and 02 demand
4. Beta blockers- Slows heart rate, decreasing 02 demand and risk for arrhythmia
5. ACE inhibitors- Decreases LV dilation by
I. Blocking vasoconstriction---decreasing preload
II. Preventing Na $ H20 buildup--decreasing preload
III. Decreases probability of LV dilation from increasing blood
volume.
6. Fibrinolysis or angioplasty-opens blocked vessel
STEMI
Percutaneous coronary intervention (preferred) or Fibrinolysis
32
What could most likely be complications of reperfusion after fibrinolysis or angioplasty?
How can reperfusion injury be demonstrated clinically?
1. CONTRACTION BAND NECROSIS- Reperfusion, calcium influx---hyper-contractions of myofibrils.
2. REPERFUSION INJURY- Generation of oxygen free radicals that further damage the myocytes after reperfusion.
By continued rise of cardiac enzymes despite better coronary blood flow
33
```
What are the changes that occur in < 4 hours after an MI?
In terms of-
1. Gross changes
2. Microscopic changes
3. Complications
```
1. No gross change seen
2. No microscopic change
3. Cardiogenic shock (massive infarction)
CHF
Arrythmias
34
```
What are the changes that occur in 4-24 hours after an MI?
In terms of-
1. Gross changes
2. Microscopic changes
4-8 hours
12-24 hours
3. Complications
```
1. Dark discoloration (dark mottling). Tetrazolium staining may identify infarction during this period w/ viable tissue red and infarcted tissue-red
2. Coagulation necrosis (removal of nuclei from cells but cells maintain structural integrity)
4-8 Hrs WAVY MYOFIBERS are seen (intact contacting fibers
tugging on dead, non-contracture fibers)
Edema separates myocardial cells
12-24 Hrs- Contraction bands at borders of infarct due to
reperfusion injury
3. Arrythmias (hypoxia decreased ATP production which in turn impairs the Na-K-ATPase pump thus altering membrane potential.
35
What are the changes that occur in 1-3 days after an MI?
In terms of-
1. Gross changes
2. Microscopic changes
3. Complication and it's clinical presentation
1. Yellow pallor (coz of the arrival of WBCs)
2. Neutrophils present, dilated vessels (hyperemia) and extensive coagulation necrosis
3. Fibrinolysis pericarditis (occurs only in transmural infarction)
and presents with chest pain and friction rub.
Fibrinolysis due to deposition of fibrin or inflammatory debris on the
pericardium
36
```
What are the changes that occur in 4-7 days after an MI?
In terms of-
1. Gross changes
2. Microscopic changes
3. Complications
```
1. Yellow pallor
2. Macrophages (phagocytose dead necrotic debris leaving the heart in its weakest state and prone to rupture)
3. Rupture of myocardial free wall (leads to cardiac tamponade)
Rupture Inter-ventricular septum (leads to shunt)
Rupture of papillary muscle (leads to valvular insufficiency or
regurgitation)
37
```
What are the changes that occur in 1-3 weeks after an MI?
In terms of-
1. Gross changes
2. Microscopic changes
3. Complications
```
1. Red border emerges as granulation tissue enters into the infarct
Yellow infarct surrounded by hyperemic red borders.
2. Granulation tissue (plump fibroblasts, collagen and blood vessels. Type I collagen
3.
38
```
What are the changes that occur in >1 month after an MI?
In terms of-
1. Gross changes
2. Microscopic changes
3. Complications
```
1. White scar
2. Fibrosis
3. Aneurysm (due to weekend cardiac muscle which has been
replaced by non-compliant scarred tissue)
Mural thrombus (due to stasis of blood in areas of aneurysm)
Dressler syndrome (autoimmune pericarditis that occurs 6-8 weeks post MI due to exposure of the immune system to pericardial antigens exposed from previous 4rm pericardial inflammation and can result in Fibrinous pericarditis.
39
What is SUDDEN CARDIAC DEATH?
Unexpected death due to cardiac disease that occur without symptoms or w/ symptoms occurring <1 hour.
40
Most common etiology for Sudden cardiac death (SCD)?
What predisposes to SCD?
Acute ischemia---ventricular arrhythmia
Indeed 90% of patients have pre-existing atherosclerosis
41
What are other less common causes of sudden cardiac death?
Mitral valve prolapse
Cardiomyopathy
Cocaine abuse
42
What is Chronic Ischemic Heart Disease?
What other heart condition can CIHD progress to?
Poor myocardial function due to chronic ischemic damage (WITH OR WITHOUT INFARCTION)
Progresses to CHF
43
What is CHF?
What are the 2 classifications of CHF?
Right sided HF
Left sided HF
44
Give examples of causes of left sided HF
```
Ischemia
MI
Hypertension
Dilated cardiomyopathy
Restrictive cardiomyopathy
```
45
What are the clinical features of left sided HF?
1. In the lungs
What is the characteristic finding of alveolar cells associated with HF? It's alias?
1. Pulmonary congestion---pulmonary edema---Dyspnea, crackles, Orthopnea, Paroxysmal nocturnal dyspnea,
Congestion of small alveolar capillaries burst--- intraalveolar hemorrhage--- HEMOSIDERIN MACROPHAGES (HF CELLS)
46
What is the relationship between CHF and the RAAS?
```
Decreased forward perfusion--- activation of RAAS--- vasoconstriction by angiotensin II
Aldosterone production (increase Na and fluid buildup)
```
Fluid buildup exacerbates the CHF.
47
1. What is the mainstay of treatment for CHF?
2. What is the pneumonic of the drugs used in the treatment of CHF?
3. What agents improve mortality in HF?
4. African Americans have been shown to benefit from this medications
1. ACE inhibitors
```
2. B-Sad (coz you have CHF)
B-Blockers
Spironolactone (K sparing diuretic)
ACE inhibitors, ARBs
Diuretics (Thiazides, furosemide), Digoxin
```
3. B-Sa (B-blockers should only be used in the long term management of patients with HFrEF but not in decompensated HFrEF)
4. H&N (Hydralazine & Nitrates)
48
What is the most common cause Right CHF?
What are other causes?
1. Left sided HF
Other causes:
- Left to right shunt
- Chronic lung diseases (Cor pulmonale)
49
What are the clinical manifestations of Right sided CHF?
What are the clinical manifestations of Left sided HF?
Right sided
1. Jugular venous distention
2. PAINFUL hepato-splenomegaly (nutmeg liver) due to distention of veins in liver. May progress to cardiac cirrhosis of liver.
3. Dependent pitting edema (increased hydrostatic pressure)
Left sided
1. Orthopnea
2. Paroxysmal nocturnal dyspnea
3. Pulmonary edema
50
1. What of these shunts presents with cyanosis shortly after birth?
R-L shunt?
L-R shunt?
2. What weeks embryogenesis does congenital defect develop?
1. R-L shunt
| 2. Week 3- Week 8
51
What is the most common congenital heart defect?
What kind of shunt is seen here?
What is the consequence of a small shunt?
What is the consequence of a large shunt?
What is its murmur? And where can it be heard?
1. VSD
2. L-R shunt
3. Small shunts are usually asymptomatic
4. Large shunts can lead to eisenmenger syndrome
5. Harsh holosystolic murmur heard at the left lower sternal border
52
Which congenital heart defect is associated with fetal alcohol syndrome?
VSD
53
What is the treatment?
Surgical closure
Small defects may close spontaneously
54
What is the most common type of ASD?
What type of shunt is seen here?
What is the type of ASD associated with Down syndrome?
1. Ostium secundum (most commonly an isolated defect)
2. L-R shunt
3. Ostium primum (are often associated with other cardiac defects)
Children with Down syndrome often have endocardial cushion defect (VSD, ASD, AV septal defect) and also have a low baseline HR
55
What is the auscultatory clinical finding in ASD?
1. Splitting of S2 (due to increased blood in right heart which delays closure of pulmonary valve)
2. Loud S1 across the upper left sternal border
- Increase L-R shunt increases volume of blood passing through the tricuspid valve over the mitral valve thereby keeping the tricuspid valve open for rapid RV filling throughout diastole so that at the onset of systole, the tricuspid valve snaps shut.
- Simultaneous decreased flow across the mitral valve makes LV filling over before diastole is over and the mitral valve cusps float together prior to systolic closure.
Just imagine closing a door against resistance (of wind) compared to closing it with no resistance, of course slamming the door shut against resistance will create a loud noise.
3. Systolic ejection murmur (due to increased blood flow along the pulmonary valve)
56
What is an important complication of ASD? (L-R shunt)
Paradoxical embolus (and have an increased risk of stroke)
57
1. What disease is associated with a PDA?
2. What kind if shunt is seen here?
3 What is the characteristic auscultatory finding in PDA.?
4. What an anatomical site is auscultation best heard?
5. Can PDA lead to eisenmenger syndrome? How?
1. Congenital rubella
2. L-R shunt
3. Holosystolic 'machine-like' murmur
4. Left infra clavicular region
5. Yes, due to long standing L-R shunt. Resulting in lower extremity cyanosis
58
What are manifestations of eisenmenger syndrome?
Reversal of L-R shunt to R-L shunt
Late cyanosis
Polycythemia
Clubbing
59
1. What is the pathology in transposition of the great arteries?
2. Does this present with early cyanosis? How?
3. What maternal disease is it associated with?
1. Pulmonary artery arises from the LV
Aorta arises from the RV
2. Yes there is early cyanosis because the pulmonary and systemic circuits do not mix and this is incompatible with life.
3. Maternal diabetes
60
What is the management for transposition of great arteries?
What is the gross sequelae of the L and R ventricles?
1. Creation of shunt after birth is required for survival as the pulmonary and systemic circuits do not mix.
2. Admin of prostaglandin E to maintain PDA till definitive surgical repair is done.
Hypertrophy of RV
Atrophy of the LV
61
What is the pathology behind truncus arteriosus?
Does this present with early cyanosis?
Failure of truncus arteriosus to divide into aorta and pulmonary artery.
Yes. Because deoxygenated blood from RV mixes with oxygenated blood before the great vessels separate.
62
What is the pathology in tricuspid atresia?
What is the gross sequelae of the RV
Which congenital heart defect is tricuspid atresia associated with?
1. Tricuspid valve fails to develop
2. Hypo-plastic RV
3. ASD with R-L shunt--- EARLY CYANOSIS
63
Describe the pathology in coarctation of the aorta
What are the two forms of coarctation of the aorta?
Narrowing of the aorta
1. Infantile form
2. Adult form
64
Where is the coarctation in the infantile form of coarctation of the aorta?
How does this condition cause cyanosis in infants?
1. Distal to the aortic arch (after the aortic arch) and proximal to the PDA (before the PDA).
Infantile form is ass with a PDA
2. Blood moving from the pulmonary artery shunts directly through the PDA into the (lower pressure) distal aorta (rather than going ahead to the lungs) due to the presence of the coarctation before the area of the PDA thus babies present with lower extremity cyanosis
65
Which genetic syndrome is associated with Coarctation if the aorta?
Turner syndrome
66
Where is the coarctation in the adult form of coarctation of the aorta?
What are the clinical findings present?
At which stage of life is this diseases classically discovered?
1. Coarctation is found after the aortic arch (no PDA in adult form)
2. HPN in the upper extremities due to increased blood surge through the arterial derivatives the aortic arch (R. Brachiocephalic A. Common carotid A. Left subclavian A.) as a result of the distal
coarctation.
Hypotension in the lower extremities with weak peripheral pulses.
3. Adulthood
67
What is the characteristic x-Ray finding in adult type coarctation of the aorta?
What valvular defect is (Adult type) coarctation of aorta associated with?
1. NOTCHING OF RIBS ON THE X-RAY
Due to the formation of collateral circulation across the intercostal arteries to compensate for HPN in these vessels.
These engorged arteries impress upon the ribs cashing notching.
2. Bicuspid aortic valve.
68
How many chambers of the heart does dilated cardiomyopathy involve?
All 4 chambers
69
Is dilated cardiomyopathy a systolic or diastolic dysfunction?
Systolic as the dilated casual muscles are weak and cannot pump effectively
70
Give 3 complications of a dilated cardiomyopathy
1. Mitral and tricuspid valve regurgitation
2. Arrhythmias- stretching and dysfunction of conducting tissues
3. Bi-ventricular CHF
71
What is the most common cause of dilated cardiomyopathy?
Idiopathic
72
What is the pattern of inheritance I'm dilated cardiomyopathy?
Autosomal dominant
73
Give 5 causes of dilated cardiomyopathy
1. Infection with coxsackie A/B (w/ dilated cardiomyopathy as a late complication)
2. Alcohol- and it's metabolites have a direct toxic effect on heart
3. Doxorubicin- a chemotherapy
4. Pregnant women in late pregnancy- soon after childbirth probably secondary to gestational HPN
5. Genetic disorder (AD)
74
What is the treatment for dilated cardiomyopathy?
Heart transplant
75
How many chambers of the heart does hypertrophic myopathy affect ?
Name
Left ventricle
76
What is the pattern of inheritance in hypertrophic cardiomyopathy?
What is the genetic defect?
1. Autosomal dominant
| 2. Genetic mutations not sarcomere proteins (beta-myosin heavy chain mutation)
77
What is a common complication of hypertrophic cardiomyopathy?
What is responsible for this complication?
1. Sudden death (in young athletes)
| 2. Ventricular arrhythmias
78
How is syncope induced by exercise associated with hypertrophic cardiomyopathy
Sub-aortic hypertrophy of the inter ventricular septum results in functional aortic stenosis.
79
What is the biopsy finding in hypertrophic cardiomyopathy?
Myofibrils hypertrophy with disarray
80
Is restrictive cardiomyopathy a systolic of diastolic cardiomyopathy?
Why?
Diastolic
Decreased compliance of ventricle reduces filling during diastole.
81
Give causes of restrictive cardiomyopathy
1. Amyloidosis- amyloid deposition
2. Sarcoidosis- granulomas
3. Hemochromatosis- excessive storage of iron in the tissues
4. Endocardial fibro-elastosis (CHILDREN)
5. Loeffler syndrome (eosinophilia--eosinophilic infiltrate--inflammation---fibrosis---restrictive cardiomyopathy
82
What is a complication of restrictive cardiomyopathy?
CHF
83
What is the characteristic ECG finding in restrictive cardiomyopathy?
Low voltage ECG & Diminished QRS amplitude.
84
What is the causative organism of acute rheumatic fever?
Group A beta hemolytic strep
85
How many weeks after a strep throat does acute rheumatic fever arise?
Which population?
1. 2-3 weeks
| 2. Children
86
What is the mechanism by which the immune system cross react with normal tissues in acute rheumatic fever?
Which specific antigen of the Group A beta hemolytic strep is responsible for this altered immune response
Molecular mimicry
Bacterial M protein (which resembles proteins in human tissue)
87
What is the diagnostic criteria for Acute rheumatic fever?
1. An evidence of past history of group A beta hemolytic strep infection (Elevated ASO, DNase beta titers)
2. Minor criteria (non-specific: fever, elevated ESR)
3. Major criteria (JONES CRITERIA)
Migratory poly-arthritis
Pancarditis
Endocarditis- Mitral valve more commonly involved
Small vegetations along closure line- regurgitate
MYOCARDITIS- most common cause of death during the
acute phase
Pericarditis- Friction rub, chest pain
Subcutaneous nodules
Erythema marginatum (annular, non-pruritic rash with erythematous borders- trunk, limbs)
Sydenham chorea (rapid, involuntary mm movement)
88
What are the characteristic cells seen in the myocardial during acute rheumatic fever?
ASCHOFF BODIES which contains
-Foci of chronic inflammation
-Anitschkow cells (reactive HISTIOCYTE with slender, wavy nuclei:
"caterpillar nuclei"
-Giant cells
-Fibrinoid material
89
What is the mechanism of myocytes damage in Chronic ischemic Heart Disease?
How does CIHD lead to dilated cardiomyopathy and CHF?
Repeated ischemic episodes leads to the replacement of contractile cardiac muscle into non-contractile fibrous tissue
The progressive replacement of cardiac tissues and buildup of fibrous tissue weakens the heart and makes it dilated. A dilated heart cannot pump effectively---CHF
90
How does CIHD lead to stable angina
Repeated infarction---release of inflammatory factors---platelets aggregation---thrombosis of vessel lumen---fixed coronary stenosis
91
Why do patients with CIHD show hibernating myocardium?
What are the Management goals for a hibernating myocardium?
1. Hibernating myocardium has reduced contractile to due to poor perfusion but remains viable. May recover with revascularization. (Persistent myocardial dysfunction due to chronic ischemia)
2. Reduce myocardial oxygen demand (beta blockers)
Restore myocardial blood flow- coronary artery bypass grafting
92
What is a stunned myocardium?
TRANSIENT myocardial dysfunction after blood flow is restored following short term ischemia.
Manifests as prolonged wall motion abnormalities days to weeks after short term ischemic attack. Resolves spontaneously
93
How many days post-MI does acute Fibrinous pericarditis occur?
What are the 3 most commonly associated symptoms associated with pericarditis?
1-3 days post (transmural) infarct due to underlying myocardial inflammation
1. Precordial pain that is relieved by leaning forwards and is exacerbated by leaning backwards
2. Pericardial friction rub
3. ST segment elevation and PR segment depression in ECG
94
A complication of MI is ventricular aneurysm and ventricular pseudo-aneurysm.
Differentiate between the 2
Left ventricular pseudo-aneurysm is a complication of MI where myocardial rupture is contains within the pericardium or granulation tissue in contrast to a true ventricular aneurysm which aneurysm is contained within the walls of the myocardium.
95
Give 4 sequelae of ventricular pseudo-aneurysm
How many days post MI are patents prone to pseudo-aneurysm formation and rupture?
1. Rupture & hemorrhage
2. Emboli formation
3. Arrhythmias
4. Cardiogenic shock
3-14 days (just memorize ;(
96
How many weeks post STEMI does VENTRICULAR ANEURYSM develop?
2 weeks- months status-post large transmural MI w/ early infarct expansion
97
What is the difference between infarct expansion and infarct extension?
Are 2 complications occurring in the early infarct period that can significant increase the functional infarct size.
INFARCT EXTENSION- Increasing the mass of necrotic tissue
INFARCT EXPANSION- thinning and dilating the infarcted zone (think of the necrotic tissue as a rubber band which expands to thin out and dilate the infarcted zone)
98
Give 3 sequelae of ventricular aneurysm
1. Arrhythmia (due to stretching and dysfunction of conducting tissues)
2. Cardiogenic shock (due to progressive inability of the heart to pump efficiently and effectively)
3. Thromboembolism (due to stasis of blood in site of aneurysm)
99
What is the name of the paradoxic systolic out-bulging which can be palpated on the chest well in patients in ventricular aneurysm?
SYSTOLIC BULGE
100
Are VENTRICULAR ANEURYSMS prone to rupture?
Why? Or Why not?
NO
Because they are lined by scar tissue.
101
In What time frame does cardiac arrhythmias typically occur after MI?
First few days
102
What is the pathological series of events in MI
1. Rupture of atherosclerotic plaque
2. Thrombosis and occlusion of coronary artery
3. Prolonged ischemia to cardiac tissues
4. Infarction
103
What are the common symptoms of Acute Coronary Syndrome?
1. Retro-sternal pain
2. Pain in the left arm/jaw
3. Diaphoresis
4. Nausea
5. Vomiting
6. Dyspnea
7. Fatigue
104
STEMI (ST Elevation MI)
1. What are the ECG findings?
2. Cardiac marker findings?
1. Persistent ST segment elevation (>1mm in 2 contiguous limb leads and >2mm in 2 contiguous chest leads) or New LBBB (Left Bundle Branch Block)
2. Increased Troponin (not required in the presence of persistent ST segment elevation)
105
NSTEMI (Non-ST Elevation MI)
1. What are the ECG findings?
2. Cardiac marker findings?
1. No ST segment elevation (ECG may be normal or show minor changes)
2. Increased Troponin- indicating onset of 24 hrs
106
Pathologic Q waves are indicative of what?
Give 4 requirements of a given Q wave to classify it as pathologic
1. An old transmural infarct
2. >1mm (40ms) wide
>2mm deep
Found in V1-V3
>25% of QRS complex
107
Which other test apart from Troponin I and CK-MB can be used to diagnose MI
What is its advantage
What is its disadvantage?
1. Serum myoglobulin
2. Arises very quickly after an MI before Troponin and CK-MB
Has a high negative predictive value if tested hours after an
MI. (If serum myoglobulin is not elevated during this period,
MI is unlikely)
3. It has low specificity (but high sensitivity)
108
What is the non-specific enzyme found in the liver, heart and skeletal muscle
AST (Aspartate transaminase)
109
What are the 5 most common congenital anomalies presenting with R-L (5 Ts)
1. Truncus arteriosus
2. Transposition of the great arteries
3. Tricuspid atresia (w/ RA-LA shunt)
4. Tetralogy of fallot
5. Total Anomalous Pulmonary Venous Return (TAPVR)
110
What increases or decreases degree of shunting in patients with R-L shunt?
INCREASES SHUNT
1. Hypo ventilation
2. Hypoxia
These processes increased pulmonary artery resistance (due to decreased O2 leading to vasoconstriction of the P. Vessels)
3. Crying
DECREASES SHUNT
1. Hypotension
2. Histamine release
3. Sepsis
111
What is the most common cyanotic congenital heart disease that presents in the neonatal period?
How does it present?
What is heard on auscultation?
What's seen on X-ray?
What is the most common cyanotic congenital heart disease that presents after the neonatal period?
1. Transposition of the great arteries
2. Presents as cyanosis within the 24 hours and not relieved by supplemental oxygen
3. Single S2 is heard on auscultation.
4. Eggs on a strong appearance
5. Tetralogy of fallot
112
1. What is Chronic Rheumatic Heart Disease?
2. What is the general gross abnormality seen in CRHD?
3. What is the gross valvular abnormality seen in ARHD?
4. Which heart valve is most commonly involved in CRHD?
5. Which valve is most commonly involved in heart disease due to wear and tear?
6. What is the gross abnormality if the mitral valve is involved?
7. What is the gross abnormality if the aortic valve is involved?
1. VALVE SCARRING as a consequence of rheumatic fever
2. Mitral stenosis with fish mouth appearance of the valves
3. Mitral regurgitation
4. Mitral valve
5. Aortic valve
6. Mitral stenosis+ thickening of the chordae tending and cusps
7. Aortic stenosis as a result of fusion of the commissures.
113
What is the major complication of CRHD?
Infectious endocarditis
114
Give 2 causes of Aortic stenosis
What is a RF in the development of non-pathologic aortic stenosis?
1. Normal wear and tear in aging population (>60y)
2. CRHD
BICUSPIC aortic valve.
115
What is the characteristic murmur heard in Aortic stenosis and why?
1. Systolic ejection click + Crescendo-decrescendo murmur
Systolic click and a result of the extra force that the LV uses to push the "stiffened and stenotic" aortic valve open.
Crescendo-decrescendo: increases pressure as blood flows through the stenosed aortic valve followed by gradually decreased in pressure
116
Give 3 complications of aortic stenosis
1. Concentric LV hypertrophy
2. Angina, syncope w/exercise
3. Microangiopathic hemolytic anemia
117
What is the treatment of aortic stenosis?
Valve replacement after the onset of complications
118
Give 2 causes of aortic regurgitation
1. Aortic root dilatation (syphilitic aneurysm, aortic dissection)
2. Valve damage (infective endocarditis)- most common cause of isolated aortic root dilation
119
What is the murmur heard in aortic regurgitation?
Early diastolic blowing murmur
120
What are the clinical manifestations of aortic regurgitation?
1. Hyper-dynamic circulation due to increased pulse pressure
Increased systolic pressure (in the aorta and other blood vessels) as more blood is pumped per beat
Decreased diastolic pressure(in the aorta) due to regurgitation of blood
2. Bounding pulse (water hammer pulse)
3. Quincke pulse (pulsating nail bed)
4. Head bobbing
121
1. What is Mitral valve prolapse (MVP)?
2. What causes MVP?
3. In which genetic conditions is MVP likely to occur?
4. Is this condition symptomatic or asymptomatic?
1. Ballooning of the mitral valve into the LA during systole
2. Myxoid degeneration of the valve which makes it floppy
3. Ehler-Danlos syndrome, Marfan syndrome
4. Asymptomatic
122
What is the murmur heard in MVP?
Explain why thus murmur is heard
MID-SYSTOLIC CLICK followed by REGURGITATION MURMUR
Mid-systolic click due to sudden ballooning of the mitral valve into the LA in mid-systole as a result on increasing LV systolic pressure which the degenerated valve leaflet can no longer accommodate.
123
Give 3 complications of MVP?
How common are these complications?
1. Infective endocarditis
2. Arrhythmias (due to stretching of the wall of the heart and disturbances in conducting tissues)
3. Mitral regurgitation
Complications are rare
124
What is mitral regurgitation?
Give causes of mitral regurgitation
Reflux of blood from the LV-LA during systole
1. MVP- a usual predisposing factor
2. LV dilatation
3. Papillary rupture after MI
4. Infective endocarditis
5. ARHD
125
What is the characteristic murmur of mitral regurgitation?
What increases the intensity of this murmur?
1. Holosystolic "blowing" murmur
2. Which increases with
- squatting (increased systemic resistance therefore LV has to generate more force to eject blood thus increasing intensity of murmur)
- Expiration (increased return to LA thus LV which increases systolic blood volume hence intensity of murmur)
126
Give complications of mitral regurgitation
Left sided HF due to volume overload
127
Give 2 differences between MVP and mitral regurgitation
1. MVP is caused by ballooning of valve leaflet(s) into the LA during mid-systole as a complication of myxoid degeneration of the valve
Mitral Regurgitation is caused by a reflux of blood from the LV-LA throughout systole
2. The murmur of MVP is a mid-systolic click followed by a regurgitation murmur while the murmur of Mitral Regurgitation is a holosystolic (blowing) murmur
128
What causes mitral stenosis?
Chronic Rheumatic Heart Disease
129
What is the murmur of mitral stenosis?
What is responsible for its characteristic sound?
Opening snap followed by diastolic rumble
Opening snap is as a result of force generated by the LA to force blood through a stenosed mitral valve
Diastolic rumble is the sound heard from LV filling as blood squeezes through the stenosed mitral valve
130
Give Complications of mitral stenosis due to LA dilatation and blood overload
Pulmonary congestion and alveolar hemorrhage
Pulmonary HPN and right-sided HF
LA dilatation--blood stasis--mural thrombi formation
Atrial fibrillation as a result of LA dilatation
131
What is the most common cause of endocarditis?
Where is it commonly found?
Strep viridans
Mouth
132
What type of endocarditis does does strep viridans cause?
Is this organism high virulence and low virulence?
What kinda of valves does this agent attach to?
Does it cause large or small vegetations in the valve?
Subacute endocarditis endocarditis-small vegetations that do not destroy the valve
Low virulence
Previously damaged valves (CHRD, MVP)
Small vegetations
133
Why are previously damaged valves at risk for bacterial infection
Damage if valves released tissue factor and collagen which attracts platelets (forming thrombotic vegetations).
Transient bacteremia leads to trapping of bacteria in the vegetations
134
What is the most common cause of endocarditis in IV drug users?
Is it a high virulence or low virulence organism?
Staph aureus
High virulence
135
What valve is most commonly affected in endocarditis in IV drug users?
Tricuspid valve
136
What kind of endocarditis is seen in IV drug users?
Acute endocarditis which damages the valve
137
Which organism is associated with endocarditis of prosthetic valves?
Does it involve large or small vegetations?
Staphylococcus epidermidis
Large vegetations
138
Give 2 organisms tart are responsible for endocarditis in patients with underlying colorectal (disease)cancer or ulcerative colitis
1. Enterococcus faecalis
| 2. Strep bovis
139
Which 5 organisms are associated with endocarditis of prosthetic valves?
HACEK organisms
```
Haemophilus
Actinobacillus
Cardiogaterium
Eikenella
Kingella
```
140
Give 6 clinical manifestations of bacterial endocardial
1. Fever
2. Murmur
3. Janeway lesions (painless erythematous lesions in palms and soles)
4. Splinter hemorrhages (due to embolization of septic vegetations)
5. Osler nodes (tender lesions on the fingers and toes)
6. Anemia of Chronic inflammation
141
What are the lab findings in endocarditis?
1. + blood cultures
2. Anemia of chronic diseases ( low Hb, low Fe, reduced MCV, increased ferritin, increased TIBC, decreased iron saturation)
142
What diagnostic modality is used toto diagnose lesions in valves?
Transesophageal echocardiogram
143
Which disease is associated with Libman-Sacks endocarditis
Is it sterile or unsterile?
What valve does it commonly grow on? And what complication of the valve does it cause?
SLE
Sterile
Mitral valve (present on the surface and undersurface of they valve) and results in mitral regurgitation.
144
What is non-bacterial thrombotic endocarditis (NBTE)
Which valve does it most commonly affect
what specific part of the valve
what valvular complication does it cause?
Sterile vegetations that arise due to a hypercoagulable state or adenocarcinoma.
Mitral valve
Along the lines of closures.
results in mitral regurgitation
145
What is dilated cardiomyopathy?
Does this result in systolic or diastolic dysfunction?
What kind of CHF does it cause?
Dilation of all four chambers of the heart
Systolic dysfunction due to inability of the ventricles to pump.
Biventricular CHD
146
What are the complications of dilated cardiomyopathy
Valvular regurgitation (due to stretching of the heart and thus the valves always from each other)
Arrhythmias (due to stretching and damage to the conduction tissues)
147
What are the most common causes of dilated cardiomyopathy?
What is the mnemonic involved?
1. Idiopathic
2. Genetic (autosomal dominant)
3. Alcohol (alcohol and it's acetaldehyde metabolites directly affects the heart)
4. Myocarditis (due to coxsackie A/B) characterized by lymphocytic infiltration in the myocardium. Dilated cardiomyopathy is a late complication. Presents wity chest pain, arrhythmia, sudden death, HF
5. Doxorubicin
6. Pregnancy (late pregnancy or months after childbirth)
```
ABCCCCDDE
Alcohol
wet Beriberi
Chagas' disease
Coxsackie A&B
peri-partum Cardiomyopathy
```
Doxorubicin, Daunorubicin
hEmochromatosis
148
What is the treatment for dilated cardiomyopathy?
Heart transplant.
149
What is hypertrophic cardiomyopathy?
Massive hypertrophy of the left ventricle which leads to its hypercontractility and non-compliance
150
What causes hypertrophic cardiomyopathy?
What gene is affected in hypertrophic cardiomyopathy?
What are the proteins encoded by these mutated genes?
Is this a systolic or diastolic disease?
Usually due to genetic mutation in sarcomere proteins- AUTOSOMAL DOMINANT
Structural elements of myocardial sarcomeres
a. Beta-myosin heavy chain
b. Myosin-binding protein C
Diastolic disease (as the ventricles cannot fill during diastole)
151
What disease is associated with sudden cardiac death in athletes?
Why?
Hypertrophic cardiomyopathy
Ventricular fibrillation secondary to hypertrophic cardiomyopathy
152
What are the clinical features of hypertrophic cardiomyopathy?
1. Decreased cardiac output
2. Sudden cardiac death
3. Syncope with exercise
153
What causes aortic stenosis-like syndrome in hypertrophic cardiomyopathy?
What is the characteristic of the murmur?
Where is this murmur found?
Subaortic hypertrophy of the ventricular septum.
Harsh systolic ejection murmur accompanied by a palpable thrill
Found at the left lower sternal border.
154
What does biopsy show in hypertrophic cardiomyopathy
Myofiber hypertrophy with disarray
155
The most commonly associated gene in dilated cardiomyopathy is?
The most common mutation X-linked dilated cardiomyopathy is?
TTN which encodes protein TITIN
Dystrophin
156
What are the clinical findings seen in dilated cardiomyopathy?
1. Low pulse pressure (If the heart is dilated and not pumping properly, there will be very little difference between the systolic and diastolic pressure in the aorta)
2. Systolic regurgitation murmur (dilated heart, valves drawn farther apart)
3. S3 heart sound due to increased diastolic filling (of regurgitated blood from LA)
157
What is the ultrasound findings of a dilated cardiomyopathy?
What is the x-Ray finding of a dilated cardiomyopathy?
1. Global cardiac enlargement
| 2. Balloon appearance of the Heart
158
What is takosubo cardiomyopathy?
Transient LV dysfunction as a result of increased catecholamines as a result of increased physical/emotional stress
159
What is the characteristic echocardiogram result in takotsubo cardiomyopathy?
Apical ballooning of the LV
160
What is the medical treatment for takotsubo cardiomyopathy?
ACE inhibitors
Diuretics
Beta blockers
Digoxin
161
What is the value of the ejection fraction in hypertrophic cardiomyopathy?
Normal. (Both systolic and diastolic pressures are both reduced significantly)
